The newsletter of the Memory Disorders Project at Rutgers University

Next time you feel stressed out, just imagine yourself in this scenario: You’re walking through the woods 50,000 years ago. As you round a blind curve on the trail, you come upon a saber-toothed tiger and her cubs. The tiger growls and crouches, ready to spring. You freeze in your tracks as the body’s “fight or flight” response kicks in with the intensity of a punch in the gut: Face flushed, blood pressure rising, nerve endings crackling, heart pounding, you leap off the trail and bolt into the forest for cover.
James L. McGaugh, Ph.D., tells the same story, but with a modern twist. A pioneering researcher in the field of human memory at the University of California, Irvine, McGaugh and his colleagues study the links between emotion, stress hormones, and the brain.

“You come around the corner,” McGaugh says, “and there’s a California mountain lion, which tend to eat people out here. Hormones—adrenaline and cortisol—are released from the adrenal gland. These both will influence the brain. In part they influence a brain region called the amygdala. The amygdala is in communication with other brain regions where memory creation occurs. The amygdala modulates the process in such a way that if the amygdala is activated and a memory is in the process of occurring, a stronger memory is made.”

A popular shorthand term for the saber-toothed tiger effect that McGaugh describes is “emotional memory.” The brain has evolved a way to make sure we remember emotionally arousing experiences. And not just bad ones: Whether it is the sight of a truck coming right at you on the highway or meeting the love of your life, emotional experiences can leave an indelible impression on the mind.

Indeed, in the case of war or other trauma, those memories may be so strong that they become pathological and bring symptoms of post-traumatic stress disorder (PTSD). By uncovering the biochemical mechanisms of how the brain selects emotional experiences for long-term storage, McGaugh and his colleagues may have found a way to prevent PTSD.

In Memory Yet Green

What did you eat for breakfast last Monday? What was the last magazine you read this month? How many bags of groceries did you bring home the last time you went shopping? Where were you when you found out that terrorists had flown planes into the World Trade Center?

The answer to the first three questions is most likely, “Who cares?” As for the fourth question, most Americans would probably be able to provide a vivid recollection of that awful day. Fortunately, our brains have the ability to filter out unimportant and trivial details. Otherwise, we would carry around a garbage can of useless memories. You don’t need to remember such things, and so you don’t. But if the experience is emotionally potent, it is deemed worthy of remembrance.

Decades of research on laboratory animals by McGaugh and many others has revealed the basic brain mechanisms of emotional memory. Emotional arousal is a form of stress, and it engages the same systems in the body as stumbling across a large-toothed predator in the forest. The body’s fight-or-flight response engages the “stress hormones” adrenaline and cortisol. Adrenaline activates the amygdala, which is a signal to the brain that something important has just occurred. Over time, a stronger and more lasting memory is created—a process called memory consolidation.

Disturbing Stories

About a decade ago, McGaugh and colleague Larry Cahill conducted two experiments that vividly demonstrated the machinery of emotional memory at work. Two different groups of people were shown a series of 12 images, each accompanied by a single sentence of narration.

One version of the story was uneventful and rather boring: A woman and her son visit the boy’s father at the hospital where he works. On the way, they witness a disaster preparedness drill featuring a simulated accident victim. The boy stays with his father and the mother goes home. End of boring story.

The second group hears a very different story while being shown the same series of images: On the way to the hospital, the boy is involved in a car accident in which his feet are severed. He’s rushed to the hospital, where surgeons reattach the injured limbs. The boy stays in the hospital and the mother goes home. Two weeks after hearing these stories, both groups were tested for their recall of specific details. The people who viewed the emotionally arousing story had significantly stronger memories for the emotional parts of the story and were therefore able to recall more specific details from the story.

Ultimately, it’s irrelevant that the emotional content—severely injured child—was negative, McGaugh emphasizes. “The more activated the amygdala is at the time learning is occurring, the better the recall will be for this information.” Had the experience involved eating an amazingly delicious chocolate cake versus a bland one, the outcome would have been the same: stronger memory for details about the delicious cake. “The amygdala is promiscuous as to the actual experience,” McGaugh says. “It’s just activated by emotional arousal. It doesn’t have to be a negative emotional experience. If it’s positive and it engages the amygdala, it will be a stronger memory.”

It stood to reason that if the influence of stress hormones on the brain could be blocked, then the amygdala would not orchestrate stronger memories of an emotional experience. To test this, Cahill and McGaugh did another experiment. Two groups of people were told the emotionally arousing version. Right before hearing the story, one of the groups was given propranolol (brand name Inderal), a type of medication called a beta-blocker. Widely used to treat heart disease, beta-blockers interfere with the effects of adrenaline on the body. In cardiac patients, this results in a slower but more efficient pumping of the heart. In the study participants, the drug would prevent stress hormones from activating the amygdala. The study found that people taking propranolol did not show stronger memories for the emotional aspects of the story. “They remembered a lot of what they saw, but they didn’t have a selectively stronger memory for the emotional content,” McGaugh explains.

Pathological Memory

The work of Cahill, McGaugh, and many others reveals something essential about how human memory works. But it also opens the door to helping people for whom emotional memory can become a living hell. By one estimate, up to 15 percent of people who have traumatic emotional experiences show symptoms of PTSD. Typical signs include intense, vivid and intrusive flashbacks or nightmares of the traumatic events, accompanied by extreme anxiety. People with the syndrome may also become emotionally numb or excessively jittery and reactive. They may go to great lengths to avoid reminders of the traumatic events. PTSD can develop after military combat, rape or other violent assault, natural disasters such as earthquakes or hurricanes, and automobile accidents.

 Importantly, PTSD does not appear, full-blown, immediately after the trauma. It takes a period of weeks to months for the symptoms to manifest themselves. It‘s generally believed that a key step in developing PTSD is repeatedly re-experiencing the event in one’s mind. Each time, the brain’s emotional memory system kicks in and strengthens the memory until it is virtually branded on the person’s consciousness. This period of time represents a potential window of opportunity for thwarting PTSD.

In a study published in 2002, Roger Pitman, M.D., a psychiatrist at Harvard Medical School and expert on PTSD, administered beta-blockers to emergency room patients within hours of experiencing trauma such as automobile accidents. The study participants received the drug for a total of 19 days. One month after the trauma, people on the medication showed fewer symptoms of PTSD. A similar experiment conducted in France had the same basic findings.

It’s too soon to start giving beta-blockers to everybody who experiences trauma. The medications have potentially harmful side effects, and more documentation of the benefits and risks is needed before psychiatrists can launch a full-scale assault on the amygdala. Pitman is currently planning a larger trial of propranolol at Massachusetts General Hospital.

One thing is clear: This research has enormous implications for the scores of people who each day suffer emotional trauma—whether because of a roadside bomb in Iraq or a fiery car wreck on the freeway. In addition to repairing fractured bones and internal injuries, emergency room physicians may someday be able to write a prescription to prevent emotional memories from becoming pathological and disabling.

Further Reading:

  • "Memory and Emotion: The Making Of Lasting Memories," by James L. McGaugh. (Columbia University Press: 2003. 162 pages, hardcover.)

Cahill, L., and McGaugh, J.L., "A Novel demonstration of enhanced memory associated with emotional arousal." (Consciousness and Cognition, 1995, Vol. 4, pp. 410-421.)

  • "B-adrenergic activation and memory for emotional events," by Larry Cahill and others. (Nature, 1994, Vol. 371, pp. 702-704.)
  • "Pilot study of secondary prevention of posttraumatic stress disorder with propranolol," By Roger K. Pitman and others. (Biological Psychiatry, 2002, Vol. 51, pp. 189-192.)